In fact, treatment with JQ1 preferentially reduced BRD4 at super-enhancers for MYC in MM cells [57] and reduced BRD4 occupancy at promoters of MYC, BCL2, and CDK6 in AML cell lines [66] while HDAC inhibitors caused a substantial increase in global acetylation of genes, resulting in translocation and redistribution of BRD4 as it binds to newly acetylated sites [67]. The gene discussed is BCL2; the disease is Miyoshi myopathy.